53BP1 Regulates DSB Repair Using Rif1 to Control 5′ End Resection

@article{Zimmermann201353BP1RD,
  title={53BP1 Regulates DSB Repair Using Rif1 to Control 5′ End Resection},
  author={Michal Zimmermann and Francisca Lottersberger and Sara C. B. Buonomo and Agnel Sfeir and Titia de Lange},
  journal={Science},
  year={2013},
  volume={339},
  pages={700 - 704}
}
Fixing Broken DNA Some physiological processes, such as immunoglobulin class switching and telomere attrition, result in double-stranded DNA breaks. The DNA damage repair protein, 53BP1, prevents nucleolytic processing of these breaks, but the proteins it partners with to do this are unknown (see the Perspective by Lukas and Lukas). Di Virgilio et al. (p. 711, published online 10 January), using mass spectroscopy–based methods, and Zimmermann et al. (p. 700, published online 10 January), using… 
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References

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53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobility
TLDR
It is proposed that the binding of 53BP1 near DNA breaks changes the dynamic behaviour of the local chromatin, thereby facilitating NHEJ repair reactions that involve distant sites, including joining of dysfunctional telomeres and AID-induced breaks in immunoglobulin class-switch recombination.
Shelterin-Like Proteins and Yku Inhibit Nucleolytic Processing of Saccharomyces cerevisiae Telomeres
TLDR
The role of key telomeric proteins in protecting budding yeast telomeres from degradation is investigated and it is shown that the Saccharomyces cerevisiae shelterin-like proteins Rif1, Rif2, and Rap1 inhibit nucleolytic processing at both de novo and native telomereres during G1 and G2 cell cycle phases.
Human CtIP promotes DNA end resection
TLDR
These findings establish evolutionarily conserved roles for CtIP-like proteins in controlling DSB resection, checkpoint signalling and homologous recombination.
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TLDR
To define the end-protection problem, the whole shelterin complex is removed from mouse telomeres through conditional deletion of TRF1 and TRF2 in nonhomologous end-joining (NHEJ) deficient cells, and two DNA damage response pathways not previously observed upon deletion of individual shelterin proteins are revealed.
DNA processing is not required for ATM-mediated telomere damage response after TRF2 deletion
TLDR
Activation of the ATM kinase pathway at chromosome ends does not require overhang degradation or other overt DNA processing, and telomere structure after conditional deletion of mouse TRF2, the protective factor at telomeres is studied.
53BP1 facilitates long-range DNA end-joining during V(D)J recombination
TLDR
A previously unrecognized defect in the joining phase of V(D)J recombination in 53BP1-deficient lymphocytes is reported that is distinct from that found in classical non-homologous-end-joining-, H2ax-, Mdc1- and Atm- deficient mice, suggesting a more general role for 53BP 1 in maintaining genomic stability during long-range joining of DNA breaks.
DNA Damage Foci at Dysfunctional Telomeres
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